bromochloroacetic-acid and Infertility

bromochloroacetic-acid has been researched along with Infertility* in 1 studies

Other Studies

1 other study(ies) available for bromochloroacetic-acid and Infertility

Article	Year
Developmental diethylstilbestrol exposure alters genetic pathways of uterine cytodifferentiation. Molecular endocrinology (Baltimore, Md.), 2005, Volume: 19, Issue:3 The formation of a simple columnar epithelium in the uterus is essential for implantation. Perturbation of this developmental process by exogenous estrogen, such as diethylstilbestrol (DES), results in uterine metaplasia that contributes to infertility. The cellular and molecular mechanism underlying this transformation event is not well understood. Here we use a combination of global gene expression analysis and a knockout mouse model to delineate genetic pathways affected by DES. Global gene expression profiling experiment revealed that neonatal DES treatment alters uterine cell fate, particularly in the luminal epithelium by inducing abnormal differentiation, characterized by the induction of stratified epithelial markers including members of the small proline-rich protein family and epidermal keratins. We show that Msx2, a homeodomain transcription factor, functions downstream of DES and is required for the proper expression of several genes in the uterine epithelium including Wnt7a, PLAP, and K2.16. Finally, Msx2-/- uteri were found to exhibit abnormal water trafficking upon DES exposure, demonstrating the importance of Msx2 in tissue responsiveness to estrogen exposure. Together, these results indicate that developmental exposure to DES can perturb normal uterine development by affecting genetic pathways governing uterine differentiation. Topics: Alkaline Phosphatase; Animals; Apoptosis; Cell Differentiation; Cell Lineage; Cell Proliferation; Cell Transformation, Neoplastic; Diethylstilbestrol; DNA Primers; DNA-Binding Proteins; DNA, Complementary; Epithelium; Estrogens, Non-Steroidal; Female; Homeodomain Proteins; In Situ Hybridization; Infertility; Keratins; Metaplasia; Mice; Mice, Knockout; Mice, Transgenic; Models, Biological; Mutation; Oligonucleotide Array Sequence Analysis; Pregnancy; Pregnancy, Animal; Prenatal Exposure Delayed Effects; Proto-Oncogene Proteins; Reverse Transcriptase Polymerase Chain Reaction; Ribonucleases; Time Factors; Transcription, Genetic; Up-Regulation; Uterus; Wnt Proteins; Wnt-5a Protein	2005

Article

Year

Developmental diethylstilbestrol exposure alters genetic pathways of uterine cytodifferentiation.

Molecular endocrinology (Baltimore, Md.), 2005, Volume: 19, Issue:3

The formation of a simple columnar epithelium in the uterus is essential for implantation. Perturbation of this developmental process by exogenous estrogen, such as diethylstilbestrol (DES), results in uterine metaplasia that contributes to infertility. The cellular and molecular mechanism underlying this transformation event is not well understood. Here we use a combination of global gene expression analysis and a knockout mouse model to delineate genetic pathways affected by DES. Global gene expression profiling experiment revealed that neonatal DES treatment alters uterine cell fate, particularly in the luminal epithelium by inducing abnormal differentiation, characterized by the induction of stratified epithelial markers including members of the small proline-rich protein family and epidermal keratins. We show that Msx2, a homeodomain transcription factor, functions downstream of DES and is required for the proper expression of several genes in the uterine epithelium including Wnt7a, PLAP, and K2.16. Finally, Msx2-/- uteri were found to exhibit abnormal water trafficking upon DES exposure, demonstrating the importance of Msx2 in tissue responsiveness to estrogen exposure. Together, these results indicate that developmental exposure to DES can perturb normal uterine development by affecting genetic pathways governing uterine differentiation.

Topics: Alkaline Phosphatase; Animals; Apoptosis; Cell Differentiation; Cell Lineage; Cell Proliferation; Cell Transformation, Neoplastic; Diethylstilbestrol; DNA Primers; DNA-Binding Proteins; DNA, Complementary; Epithelium; Estrogens, Non-Steroidal; Female; Homeodomain Proteins; In Situ Hybridization; Infertility; Keratins; Metaplasia; Mice; Mice, Knockout; Mice, Transgenic; Models, Biological; Mutation; Oligonucleotide Array Sequence Analysis; Pregnancy; Pregnancy, Animal; Prenatal Exposure Delayed Effects; Proto-Oncogene Proteins; Reverse Transcriptase Polymerase Chain Reaction; Ribonucleases; Time Factors; Transcription, Genetic; Up-Regulation; Uterus; Wnt Proteins; Wnt-5a Protein

2005